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Abstract

Abstract

Hypertension is strongly assosiated with obesity [73]. According to the Framingham study 78% of essential hypertension in men, and 65 % of essential hypertension in women can be directly attributed to obesity [94]. As the amount of obesity increases all over the world, the aspect of how to treat obesity-related hypertension becomes more and more relevant. Both BMI and waist-to-hip ratio are positively associated with development of hypertension, altough the latter seems more important. Several humoral and metabolic mechanisms may be

involved in the development of hypertension in obesity. Such as increased reabsorption of sodium in the kidneys causing increase in plasma volume, renal structural changes, increased activity of the renin-angiotensin-aldosterone system, increased sympathetic nervous system activity with increased levels of especially norepinephrine, insulin resistance and hyperinsulinemia, increased level of circulating leptin and leptin resistance, increased level of

cortisol as a consequence of chronically exposure to mental stress, decreased ability to vasodilatory response to mental/physical stress, endothelial dysfunction and genetical predisposition.

The Norwegian Government decided in 2004 that thiazides should be the first choice medicine in the treatment of hypertension in Norway. When looking deeply into the possible pathophysiological mechanisms in obesity-hypertension through several publications, we question whether this is the best treatment of this group of hypertensives. Sharma et al [107] suggest that ACE-inhibitors should be the drug of choice for obese hypertensive subjects, because they possess many different mechanisms leading to the antihypertensive effect [197].

In addition they have positive effects on metabolic impairment as they improve the insulin sensitivity and is have no negative effects on fatmetabolism [107], but further investigation is necessary before firm guidelines can be made.